Antigenotoxic Studies of Different Substances to Reduce the DNA Damage Induced by Aflatoxin B1 and Ochratoxin A

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Abstract

Mycotoxins are produced mainly by the mycelial structure of filamentous fungi, or more specifically, molds. These secondary metabolites are synthesized during the end of the exponential growth phase and appear to have no biochemical significance in fungal growth and development. The contamination of foods and feeds with mycotoxins is a significant problem for the adverse effects on humans, animals, and crops that result in illnesses and economic losses. The toxic effect of the ingestion of mycotoxins in humans and animals depends on a number of factors including intake levels, duration of exposure, toxin species, mechanisms of action, metabolism, and defense mechanisms. In general, the consumption of contaminated food and feed with mycotoxin induces to neurotoxic, immunosuppressive, teratogenic, mutagenic, and carcinogenic effect in humans and/or animals. The most significant mycotoxins in terms of public health and agronomic perspective include the aflatoxins, ochratoxin A (OTA), trichothecenes, fumonisins, patulin, and the ergot alkaloids. Due to the detrimental effects of these mycotoxins, several strategies have been developed in order to reduce the risk of exposure. These include the degradation, destruction, inactivation or removal of mycotoxins through chemical, physical and biological methods. However, the results obtained with these methods have not been optimal, because they may change the organoleptic characteristics and nutritional values of food. Another alternative strategy to prevent or reduce the toxic effects of mycotoxins is by applying antimutagenic agents. These substances act according to several extra- or intracellular mechanisms, their main goal being to avoid the interaction of mycotoxins with DNA; as a consequence of their action, these agents would inhibit mutagenesis and carcinogenesis. This article reviews the main strategies used to control AFB ₁ and ochratoxin A and contains an analysis of some antigenotoxic substances that reduce the DNA damage caused by these mycotoxins.

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J W Bennett, M A Klich (2003)

Mycotoxins are secondary metabolites produced by microfungi that are capable of causing disease and death in humans and other animals. Because of their pharmacological activity, some mycotoxins or mycotoxin derivatives have found use as antibiotics, growth promotants, and other kinds of drugs; still others have been implicated as chemical warfare agents. This review focuses on the most important ones associated with human and veterinary diseases, including aflatoxin, citrinin, ergot akaloids, fumonisins, ochratoxin A, patulin, trichothecenes, and zearalenone.

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Strategies to prevent mycotoxin contamination of food and animal feed: a review.

Işil Var, Alan D. W. Dobson, Bulent Kabak (2005)

Mycotoxins are fungal secondary metabolites that have been associated with severe toxic effects to vertebrates produced by many important phytopathogenic and food spoilage fungi including Aspergillus, Penicillium, Fusarium, and Alternaria species. The contamination of foods and animal feeds with mycotoxins is a worldwide problem. We reviewed various control strategies to prevent the growth of mycotoxigenic fungi as well as to inhibit mycotoxin biosynthesis including pre-harvest (resistance varieties, field management and the use of biological and chemical agents), harvest management, and post-harvest (improving of drying and storage conditions, the use of natural and chemical agents, and irradiation) applications. While much work in this area has been performed on the most economically important mycotoxins, aflatoxin B(1) and ochratoxin A much less information is available on other mycotoxins such as trichothecenes, fumonisin B(1), zearalenone, citrinin, and patulin. In addition, physical, chemical, and biological detoxification methods used to prevent exposure to the toxic and carcinogenic effect of mycotoxins are discussed. Finally, dietary strategies, which are one of the most recent approaches to counteract the mycotoxin problem with special emphasis on in vivo and in vitro efficacy of several of binding agents (activated carbons, hydrated sodium calcium aluminosilicate, bentonite, zeolites, and lactic acid bacteria) have also been reviewed.

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Much progress has been made in elucidating the biochemical and molecular mechanisms that underlie aflatoxin carcinogenesis. In humans, biotransformation of AFB1 to the putative carcinogenic intermediate. AFB-8,9-exo-epoxide, occurs predominantly by cytochromes P450 1A2 and 3A4, with the relative importance of each dependent upon the relative magnitude of expression of the respective enzymes in liver. Genetic variability in the expression of these and other cytochromes P450 may result in substantial interindividual differences in susceptibility to the carcinogenic effects of aflatoxins. Detoxification of AFB-8,9-epoxide by a specific alpha class glutathione S-transferase is an important protective mechanism in mice, and it accounts for the resistance of this species to the carcinogenic effects of AFB. This particular form of GST is expressed constitutively only at low levels in rats, but it is inducible by antioxidants such as ethoxyquin, and it accounts for much of the chemoprotective effects of a variety of substances, including natural dietary components that putatively act via an "antioxidant response element" (ARE). In humans, the constitutively expressed GSTs have very little activity toward AFB1-8,9-exo-epoxide, suggesting that--on a biochemical basis--humans should be quite sensitive to the genotoxic effects of aflatoxins. If a gene encoding a high aflatoxin-active form of GST is present in the human genome, but is not constitutively expressed, and is inducible by dietary antioxidants (as occurs in rats), then chemo- and/or dietary intervention measures aimed at inducing this enzyme could be highly effective. However, as it is possible that human CYP 1A2 may also be inducible by these same chemicals (because of the possible presence of an ARE in this gene), the ultimate consequence of dietary treatment with chemicals that induce biotransformation enzymes via an ARE is uncertain. The balance of the rate of activation (exo-epoxide production) to inactivation (GST conjugation plus other P450-mediated non-epoxide oxidations) may be a strong indicator of individual and species susceptibility to aflatoxin carcinogenesis, if the experimental conditions are reflective of true dietary exposures. There is strong evidence that AFB-8,9-exo-epoxide binds to G:C rich regions of DNA, forming an adduct at the N7-position of guanine. Substantial evidence demonstrates that AFB1-8,9-epoxide can induce activating mutations in the ras oncogene in experimental animals, primarily at codon 12.(ABSTRACT TRUNCATED AT 400 WORDS)

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Author and article information

Journal

Journal ID (nlm-ta): Toxins (Basel)

Journal ID (publisher-id): toxins

Title: Toxins

Publisher: MDPI

ISSN (Electronic): 2072-6651

Publication date Collection: April 2010

Publication date (Electronic): 19 April 2010

Volume: 2

Issue: 4

Pages: 738-757

Affiliations

[1 ]Instituto de Ciencias de la Salud, Universidad Autónoma del Estado de Hidalgo., Ex-Hacienda de la Concepción. Tilcuautla. Pachuca de Soto, Hidalgo. CP 42080, México; Email: jmorales101@ 123456yahoo.com.mx (J.A.M.); nvargas_mendoza@ 123456hotmail.com (N.V.); pattyreyes_1@ 123456hotmail.com (P.R.); crzjms@ 123456msn.com (S.C.); teresumaya@ 123456hotmail.com (T.S.)

[2 ]Laboratorio de Genética, Escuela Nacional de Ciencias Biológicas, I.P.N., Av. Wilfrido Massieu. Unidad A. López Mateos. Zacatenco. Col Lindavista. D.F. CP 07738, México; Email: eduardo.madrigal@ 123456lycos.com (E.M.B.)

[3 ]Laboratorio de Toxicología Preclínica, Escuela Nacional de Ciencias Biológicas, I.P.N., Av. Wilfrido Massieu. Unidad A. López Mateos. Zacatenco. Col Lindavista. D.F. CP 07738, México; Email: pastenrich@ 123456yahoo.com.mx (R.P.)

Author notes

[* ] Author to whom correspondence should be addressed; Email: eomsmx@ 123456yahoo.com.mx ; Tel.: +01 771 71 720 00; Fax: +01 771 71 720 00-5111.

Article

Publisher ID: toxins-02-00738

DOI: 10.3390/toxins2040738

PMC ID: 3153197

PubMed ID: 22069607

SO-VID: 2c6bdd20-e8f5-4c7f-a712-4292f181b619

License:

This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

History

Date received : 21 March 2010

Date revision received : 08 April 2010

Date accepted : 13 April 2010

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